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Effects of short-term exposure to inhalable particulate matter on telomere length, telomerase expression, and telomerase methylation in steel workers.

Dioni L, Hoxha M, Nordio F, Bonzini M, Tarantini L, Albetti B, Savarese A, Schwartz J, Bertazzi PA, Apostoli P, Hou L, Baccarelli A - Environ. Health Perspect. (2010)

Bottom Line: LTL was significantly increased in postexposure (mean ± SD, 1.43 ± 0.51) compared with baseline samples (1.23 ± 0.28, p-value < 0.001).We found no exposure-related differences in the methylation of any of the CpG sites investigated in the hTERT promoter.The LTL increase did not appear to be mediated by PM-related changes in hTERT expression and methylation.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Environmental Epigenetics, Department of Preventive Medicine, University of Milan and IRCCS Ca' Granda Maggiore Policlinico Hospital Foundation, Milan, Italy.

ABSTRACT

Background: Shortened leukocyte telomere length (LTL) is a marker of cardiovascular risk that has been recently associated with long-term exposure to ambient particulate matter (PM). However, LTL is increased during acute inflammation and allows for rapid proliferation of inflammatory cells. Whether short-term exposure to proinflammatory exposures such as PM increases LTL has never been evaluated.

Objectives: We investigated the effects of acute exposure to metal-rich PM on blood LTL, as well as molecular mechanisms contributing to LTL regulation in a group of steel workers with high PM exposure.

Methods: We measured LTL, as well as mRNA expression and promoter DNA methylation of the telomerase catalytic enzyme gene [human telomerase reverse transcriptase (hTERT)] in blood samples obtained from 63 steel workers on the first day of a workweek (baseline) and after 3 days of work (postexposure).

Results: LTL was significantly increased in postexposure (mean ± SD, 1.43 ± 0.51) compared with baseline samples (1.23 ± 0.28, p-value < 0.001). Postexposure LTL was positively associated with PM₁₀ (β = 0.30, p-value = 0.002 for 90th vs. 10th percentile exposure) and PM₁ (β = 0.29, p-value = 0.042) exposure levels in regression models adjusting for multiple covariates. hTERT expression was lower in postexposure samples (1.31 ± 0.75) than at baseline (1.68 ± 0.86, p-value < 0.001), but the decrease in hTERT expression did not show a dose-response relationship with PM. We found no exposure-related differences in the methylation of any of the CpG sites investigated in the hTERT promoter.

Conclusions: Short-term exposure to PM caused a rapid increase in blood LTL. The LTL increase did not appear to be mediated by PM-related changes in hTERT expression and methylation.

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Related in: MedlinePlus

Within-subject changes in LTL between the first day of a workweek (baseline) and after 3 days of work (postexposure). Individuals were categorized according to tertiles of PM10 exposure.
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f1-ehp-119-622: Within-subject changes in LTL between the first day of a workweek (baseline) and after 3 days of work (postexposure). Individuals were categorized according to tertiles of PM10 exposure.

Mentions: LTL showed a significant increase from baseline (n = 57; 1.23 ± 0.28 T/S relative units) to postexposure (n = 57; 1.43 ± 0.51; p < 0.001; Table 1). Figure 1 shows the changes of individuals’ LTL between the first day of a workweek (baseline) and after 3 days of work (postexposure). LTL was significantly increased both in current smokers (n = 21; baseline: 1.26 ± 0.30 T/S relative units; postexposure: 1.5 ± 0.58; p < 0.0001) and in nonsmokers (n = 36; baseline: 1.21 ± 0.27; postexposure: 1.39 ± 0.52; p = 0.002). As a sensitivity analysis, we repeated the baseline versus postexposure comparison after excluding the three subjects with the highest postexposure LTL values and found that the increase in LTL was still highly significant (baseline: 1.22 ± 0.28; postexposure: 1.34 ± 0.35; p = 0.001).


Effects of short-term exposure to inhalable particulate matter on telomere length, telomerase expression, and telomerase methylation in steel workers.

Dioni L, Hoxha M, Nordio F, Bonzini M, Tarantini L, Albetti B, Savarese A, Schwartz J, Bertazzi PA, Apostoli P, Hou L, Baccarelli A - Environ. Health Perspect. (2010)

Within-subject changes in LTL between the first day of a workweek (baseline) and after 3 days of work (postexposure). Individuals were categorized according to tertiles of PM10 exposure.
© Copyright Policy - public-domain
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3094411&req=5

f1-ehp-119-622: Within-subject changes in LTL between the first day of a workweek (baseline) and after 3 days of work (postexposure). Individuals were categorized according to tertiles of PM10 exposure.
Mentions: LTL showed a significant increase from baseline (n = 57; 1.23 ± 0.28 T/S relative units) to postexposure (n = 57; 1.43 ± 0.51; p < 0.001; Table 1). Figure 1 shows the changes of individuals’ LTL between the first day of a workweek (baseline) and after 3 days of work (postexposure). LTL was significantly increased both in current smokers (n = 21; baseline: 1.26 ± 0.30 T/S relative units; postexposure: 1.5 ± 0.58; p < 0.0001) and in nonsmokers (n = 36; baseline: 1.21 ± 0.27; postexposure: 1.39 ± 0.52; p = 0.002). As a sensitivity analysis, we repeated the baseline versus postexposure comparison after excluding the three subjects with the highest postexposure LTL values and found that the increase in LTL was still highly significant (baseline: 1.22 ± 0.28; postexposure: 1.34 ± 0.35; p = 0.001).

Bottom Line: LTL was significantly increased in postexposure (mean ± SD, 1.43 ± 0.51) compared with baseline samples (1.23 ± 0.28, p-value < 0.001).We found no exposure-related differences in the methylation of any of the CpG sites investigated in the hTERT promoter.The LTL increase did not appear to be mediated by PM-related changes in hTERT expression and methylation.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Environmental Epigenetics, Department of Preventive Medicine, University of Milan and IRCCS Ca' Granda Maggiore Policlinico Hospital Foundation, Milan, Italy.

ABSTRACT

Background: Shortened leukocyte telomere length (LTL) is a marker of cardiovascular risk that has been recently associated with long-term exposure to ambient particulate matter (PM). However, LTL is increased during acute inflammation and allows for rapid proliferation of inflammatory cells. Whether short-term exposure to proinflammatory exposures such as PM increases LTL has never been evaluated.

Objectives: We investigated the effects of acute exposure to metal-rich PM on blood LTL, as well as molecular mechanisms contributing to LTL regulation in a group of steel workers with high PM exposure.

Methods: We measured LTL, as well as mRNA expression and promoter DNA methylation of the telomerase catalytic enzyme gene [human telomerase reverse transcriptase (hTERT)] in blood samples obtained from 63 steel workers on the first day of a workweek (baseline) and after 3 days of work (postexposure).

Results: LTL was significantly increased in postexposure (mean ± SD, 1.43 ± 0.51) compared with baseline samples (1.23 ± 0.28, p-value < 0.001). Postexposure LTL was positively associated with PM₁₀ (β = 0.30, p-value = 0.002 for 90th vs. 10th percentile exposure) and PM₁ (β = 0.29, p-value = 0.042) exposure levels in regression models adjusting for multiple covariates. hTERT expression was lower in postexposure samples (1.31 ± 0.75) than at baseline (1.68 ± 0.86, p-value < 0.001), but the decrease in hTERT expression did not show a dose-response relationship with PM. We found no exposure-related differences in the methylation of any of the CpG sites investigated in the hTERT promoter.

Conclusions: Short-term exposure to PM caused a rapid increase in blood LTL. The LTL increase did not appear to be mediated by PM-related changes in hTERT expression and methylation.

Show MeSH
Related in: MedlinePlus